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GoPubMed Proteins lists recent and important papers and reviews for proteins. Page last changed on 25 Jan 2016.

Ataxia telangiectasia mutated homolog

Atm
serine/threonine protein kinase; critical regulator of the cellular DNA damage response [RGD, Feb 2006] (from NCBI)
Top mentioned proteins: p53, CAN, V1a, HAD, p21
Papers on Atm
Mutation of ataxia-telangiectasia mutated is associated with dysfunctional glutathione homeostasis in cerebellar astroglia.
New
Mayer-Pröschel et al., Rochester, United States. In Glia, 29 Feb 2016
Here we focus on the role of astroglia in ataxia-telangiectasia (A-T), a disease caused by mutations in the ataxia-telangiectasia mutated (ATM) gene.
Low-dose irradiation prior to bone marrow transplantation results in ATM activation and increased lethality in Atm-deficient mice.
New
Schubert et al., Frankfurt am Main, Germany. In Bone Marrow Transplant, 11 Feb 2016
Repopulation with ATM-competent bone marrow-derived cells (BMDCs) significantly prolonged the lifespan and improved the phenotype of Atm-deficient mice.
Microsatellite instability detected in tumor-related genes in C57BL/6J mice with thymic lymphoma induced by N-methyl-N-nitrosourea.
New
Chen et al., Beijing, China. In Mutat Res, 31 Dec 2015
MSI loci in intronic regions of Atm, Msh6 and p21 and MSI in the 3'UTR of Pms2 were detected in MNU-treated mice.
Alteration in 5-hydroxymethylcytosine-mediated epigenetic regulation leads to Purkinje cell vulnerability in ATM deficiency.
New
Li et al., Kunming, China. In Brain, 31 Dec 2015
A long-standing mystery surrounding ataxia-telangiectasia is why it is mainly cerebellar neurons, Purkinje cells in particular, that appear vulnerable to ATM deficiency.
A novel mouse model for ataxia-telangiectasia with a N-terminal mutation displays a behavioral defect and a low incidence of lymphoma but no increased oxidative burden.
New
Mayer-Pröschel et al., Rochester, United States. In Hum Mol Genet, 15 Dec 2015
Ataxia-telangiectasia (A-T) is a rare multi-system disorder caused by mutations in the ATM gene.
Defining ATM-independent Functions of the Mre11 Complex with a Novel Mouse Model.
New
Petrini et al., Kettering, United States. In Mol Cancer Res, 04 Dec 2015
UNASSIGNED: The Mre11 complex (Mre11, Rad50 and Nbs1) occupies a central node of the DNA damage response (DDR) network, and is required for ATM activation in response to DNA damage.
Differential DNA damage signalling and apoptotic threshold correlate with mouse epiblast-specific hypersensitivity to radiation.
New
Blasi et al., Milano, Italy. In Development, Dec 2015
Although upstream Atm/Atr global activity and specific γH2AX phosphorylation are similar in all cell types of the embryo, 53BP1 recruitment at DNA breaks is immediately amplified only in epiblast cells after ionizing radiation.
Simultaneous depletion of Atm and Mdl rebalances cytosolic Fe-S cluster assembly but not heme import into the mitochondrion of Trypanosoma brucei.
New
Lukeš et al., České Budějovice, Czech Republic. In Febs J, Nov 2015
ABC transporter mitochondrial 1 (Atm1) and multidrug resistance-like 1 (Mdl) are mitochondrial ABC transporters.
Low levels of endogenous or X-ray-induced DNA double-strand breaks activate apoptosis in adult neural stem cells.
New
Jeggo et al., Burgess Hill, United Kingdom. In J Cell Sci, Nov 2015
We used mice with a hypomorphic mutation in DNA ligase IV (Lig4(Y288C)), ataxia telangiectasia mutated (Atm(-/-)) and double mutant Atm(-/-)/Lig4(Y288C) mice.
DNA damage primes the type I interferon system via the cytosolic DNA sensor STING to promote anti-microbial innate immunity.
New
Impact
Gekara et al., Umeå, Sweden. In Immunity, Mar 2015
Dysfunction in Ataxia-telangiectasia mutated (ATM), a central component of the DNA repair machinery, results in Ataxia Telangiectasia (AT), a cancer-prone disease with a variety of inflammatory manifestations.
Dysregulation of the DNA Damage Response and KMT2A Rearrangement in Fetal Liver Hematopoietic Cells.
Takagi et al., Tokyo, Japan. In Plos One, 2014
However, Kmt2a (Mll)-rearranged fusion mRNA was detected in Atm-knockout mice, which are defective in the DNA damage response, but not in wild-type mice.
Anthracyclines induce DNA damage response-mediated protection against severe sepsis.
Impact
Moita et al., Lisbon, Portugal. In Immunity, 2013
This salutary effect is strictly dependent on the activation of DNA damage response and autophagy pathways in the lung, as demonstrated by deletion of the ataxia telangiectasia mutated (Atm) or the autophagy-related protein 7 (Atg7) specifically in this organ.
Expression pattern of ataxia telangiectasia mutated (ATM), p53, Akt, and glycogen synthase kinase-3β in the striatum of rats treated with 3-nitropropionic acid.
GeneRIF
Pelegrí et al., Barcelona, Spain. In J Neurosci Res, 2012
We examined whether cellular expression of ataxia telangiectasia mutated, p53, Akt, and glycogen synthase kinase-3beta, were involved in the striatal neurodegeneration in the brains of rats
Pathological neoangiogenesis depends on oxidative stress regulation by ATM.
Impact
Kubota et al., Tokyo, Japan. In Nat Med, 2012
The ataxia telangiectasia mutated (ATM) kinase, a master regulator of the DNA damage response (DDR), acts as a barrier to cellular senescence and tumorigenesis.
Wip1-dependent regulation of autophagy, obesity, and atherosclerosis.
Impact
Bulavin et al., Singapore, Singapore. In Cell Metab, 2012
Here, we show that Wip1 phosphatase, a known negative regulator of Atm-dependent signaling, plays a major role in controlling fat accumulation and atherosclerosis in mice; specifically, Wip1 deficiency prevents both conditions.
Nuclear accumulation of HDAC4 in ATM deficiency promotes neurodegeneration in ataxia telangiectasia.
Impact
Herrup et al., United States. In Nat Med, 2012
Here we report that ataxia telangiectasia mutated (ATM) deficiency causes nuclear accumulation of histone deacetylase 4 (HDAC4) in neurons and promotes neurodegeneration.
Common variants near ATM are associated with glycemic response to metformin in type 2 diabetes.
Impact
GeneRIF
Pearson et al., Dundee, United Kingdom. In Nat Genet, 2011
ATM, a gene known to be involved in DNA repair and cell cycle control, plays a role in the effect of metformin upstream of AMP-activated protein kinase, and variation in this gene alters glycemic response to metformin
ATM is involved in cell-cycle control through the regulation of retinoblastoma protein phosphorylation.
GeneRIF
Camins et al., Barcelona, Spain. In J Cell Biochem, 2010
These data demonstrate how a new molecular network on ATM regulates the cell cycle through the control of pRb phosphorylation.
Myc is required for activation of the ATM-dependent checkpoints in response to DNA damage.
GeneRIF
Frisan et al., Stockholm, Sweden. In Plos One, 2009
data demonstrate that MYC contributes to the activation of the ATM-dependent checkpoint responses, leading to cell death in response to specific genotoxic stimuli
The ataxia protein sacsin is a functional co-chaperone that protects against polyglutamine-expanded ataxin-1.
GeneRIF
Chapple et al., London, United Kingdom. In Hum Mol Genet, 2009
Sacsin knockdown resulted in a reduction in cells expressing polyglutamine-expanded ataxin.
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